Genistein Induced Apotosis in Human Gastric Carcinoma Cells

2011 ◽  
Vol 183-185 ◽  
pp. 1283-1286 ◽  
Author(s):  
Ying Liu ◽  
Xiao Mei Li
Keyword(s):  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Caspase 3 ◽  
Morphological Changes ◽  
Chromatin Condensation ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
Crescent Formation ◽  
Gastric Carcinoma Cell ◽  
Genistein Treatment

The apoptosis in gastric cancer cells induced by genistein and the relationship between this apoptosis and expression of NF-κB and Caspase-3 were studied. In vitro experiments, MTT assay was used to determine the cell growth inhibitory rate. Transmission fluorescence microscope, transmission electron microscopy, DNA-fragment assay were used to qualitively detect the apoptosis status of gastric cancer line SGC-7901 before and after the genistein treatment. Immunohistochemical staining and Western Blotting were performed to detect the expression of gene NF-κB and Caspase-3. The results showed that genistein inhibited the growth of gastric carcinoma cell line SGC-7901 in a dose-and time-dependent manner. Genistein induced SGC-7901 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation, nucleus fragmentation and apoptotic body formation. Genistein could reduce the expression of gene NF-κB, and improve the expression of gene Caspase-3.

Chrysin Alters microRNAs Expression Levels in Gastric Cancer Cells: Possible Molecular Mechanism

Drug Research ◽  
2017 ◽  
Vol 67 (09) ◽  
pp. 509-514 ◽  
Author(s):  
Farideh Mohammadian ◽  
Younes Pilehvar-Soltanahmadi ◽  
Shahriar Alipour ◽  
Mehdi Dadashpour ◽  
Nosratollah Zarghami
Keyword(s):  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Molecular Mechanisms ◽  
Gastric Cancer Cells ◽  
Gastric Carcinoma Cell ◽  
Expression Levels ◽  
Mirnas Expression ◽  
Chemopreventive Activity

Abstract Background Gastric carcinoma still remains the second most common cause of cancer mortality in the world. Chrysin, as a flavone, has showed cancer chemopreventive activity. The cellular and molecular mechanisms of chrysin in cancer cells have not been fully understood. Objective In this study, we investigate expression levels of let-7a, miR-9, mir-18a, miR-21, miR-22, miR-34a, miR-126 and mir-221 to describe the anti-cancer effects of chrysin. Materials and Methods The cytotoxic effects of chrysin were assessed using MTT assay. The effect of chrysin on the microRNAs expression was determined by qRT-PCR. Results The MTT results for different concentrations of chrysin at different times on the Gastric carcinoma cells showed that IC50 for chrysin was 68.24 µM after 24 h of treatment. Expression analysis identified that miR-18, miR-21 and miR-221 were down regulated whereas let-7a, miR-9, miR-22, miR-34a and miR-126 were up regulated in Gastric carcinoma cell line (p<0.05). Conclusion Treatment with chrysin can alter the miRNAs expression and these findings might be an explanation for molecular mechanism of chrysin effect on gastric cancer.

Antitumorigenic effect of plumbagin by induction of SHP1 in human gastric carcinoma cell lines.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 74-74
Author(s):  
Jin Sung Koh ◽  
Jong-Jae Park ◽  
Moon Kyung Joo ◽  
Hyo Soon Yoo ◽  
Jiwon Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Cancer Cells ◽  
Cell Line ◽  
Carcinoma Cell ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Gastric Carcinoma Cell ◽  
Stat3 Pathway

74 Background: Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) is a plant-drived natural agent extracted from the root of Plumbago zeylanic. A recent study reported that plumbagin down-regulated the activity of Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway to show various anti-tumor effects. We aimed in this in vitrostudy to demonstrate the inhibition of JAK2-STAT3 pathway by plumbagin through inducing SH2-containing protein tyrosine phosphatase 1 (SHP1) expression in gastric cancer cell line. Methods: We performed Wetern blot to measure SHP1, phospho-JAK2/STAT3 level, and reverse transcriptase-polymerase chain reaction (RT-PCR) to evaluate target gene expression of STAT3. Several functional studies such as water soluble tetrazolium-1 (WST-1) assay, wound closure assay and matrigel invasion assay were also performed. Results: Plumbagin induced SHP1 expression and simultaneously down-regulated phospho-JAK2/STAT3 level via dose-and time-dependant manner in MKN28 cell, a gastric carcinoma cell line which has negative SHP1 expression. This effect was consistent when JAK2-STAT3 signaling was activated by interleukin-6, and ameliorated when cells were treated with prevanadate, a protein tyrosin phosphatase inhibitor. Furthermore, plumbagin significantly reduced gene expression of cyclin D1, VEGF1, survivin, MMP9, known target products of STAT3 activation in gastric cancinogenesis. The functional effect of plumbagin could be validated as inhibition of cell proliferation, migration and invasion, which are the results of activation of JAK2-STAT3 pathway in gastric cancer cells. Conclusions: Plumbagin is a potential negative regulator of cellular growth, migration and invasion by inhibiting both constitutive and inducible STAT3 activity through induction of SHP1 in gastric cancer cells.

scholarly journals Procyanidin B2 induces apoptosis and autophagy in gastric cancer cells by inhibiting Akt/mTOR signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yuqin Li ◽  
Xiaolan Lu ◽  
Peiying Tian ◽  
Kai Wang ◽  
Jianping Shi
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Mtor Signaling ◽  
Therapeutic Drug ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Mtor Signaling Pathway ◽  
Gastric Cancer Cells

Abstract Background Procyanidin B2 (PB2), a unique component of the grape seed and other medicinal plants. PB2 has shown wide anticancer activity in various human cancer cells. However, it remains unclear about the biological effects and associated mechanisms of PB2 on gastric cancer cells. Methods Cell proliferation was measured by CCK8 assay, and cellular lactate dehydrogenase (LDH) release was measured in the culture medium. Cellular apoptosis was observed via TUNEL staining assay and measured by caspase-3 and -9 activities. Autophagy was observed by LC3 staining. Western blot analysis was performed to verify autophagy-associated proteins (Beclin1 and Atg5) and Akt-mTOR pathway. Results PB2 reduced the viability of BGC-823 and SGC-7901 cells in a concentration-dependent manner. Furthermore, PB2 induced increased apoptosis rate of gastric cancer cells and enhanced caspase-3 and -9 activities. Simultaneously, PB2 triggered autophagy in gastric cancer cells, with enhanced LC3 staining and increased expression of Beclin1 and Atg5, while the inhibition of autophagy by 3-MA reversed the PB2-induced suppression on cell viability. In addition, PB2 significantly decreased p-Akt and p-mTOR protein expression of gastric cancer cells. Conclusion PB2 exerts anti-proliferative and apoptotic effects and induces autophagy by modulating Akt/mTOR signaling pathway. PB2 may be developed as a potential therapeutic drug for gastric cancer.

scholarly journals Hop-derived Xanthohumol Induces HL-60 Leukemia Cells Death

2020 ◽  
pp. 61-72
Author(s):  
M. Pacurari ◽  
H. Brown ◽  
A. Rieland
Keyword(s):  
Cell Viability ◽  
Cell Cycle Progression ◽  
Caspase 3 ◽  
Morphological Changes ◽  
Chromatin Condensation ◽  
Dependent Manner ◽  
Cycle Progression ◽  
Humulus Lupulus L ◽  
Additional Chemotherapy ◽  
Dose Dependent

Background: Acute promyelocytic leukemia (APL) affects both kids and adults, however it is more prevalent in younger population. Although APL has a favorable prognostic, patients that relapse often do not respond positively to additional chemotherapy. Therefore, there is a need to further identify ways to overcome these challenges.  Hypothesis: In this study, we examined antileukemic effects of xanthohumol (XN), a prenylated flavonoid derived from hops (Humulus lupulus L), on human promyelocytic HL-60 cells.  Materials and Methods: HL-60 cells were exposed to different concentrations of XN (μM) for 24 h. Cell viability, cell morphology, chromatin condensation, cPARP-1 level, and caspase-3 activation, and the expression of p21WAF1/Cip1 were analyzed. Results: XN reduced HL-60 cell viability in a dose-dependent manner. XN induced a dose-dependent morphological changes including cell shrinkage and blebbing, and significantly increased the number of cells with condensed chromatin. XN significantly increased the level of cPARP-1, active caspase-3, and the expression of p21WAF/CIP mRNA. Conclusion: These data indicate that XN induces HL-60 cell death by regulating cell cycle progression and apoptosis. This study suggests that XN may have antileukemic preventive effects.

scholarly journals Curcumin inhibits the lymphangiogenesis of gastric cancer cells by inhibiton of HMGB1/VEGF-D signaling

2019 ◽  
Vol 33 ◽  
pp. 205873841986160 ◽  
Author(s):  
Wei Da ◽  
Jing Zhang ◽  
Rui Zhang ◽  
Jinshui Zhu
Keyword(s):  
Gastric Cancer ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Morphological Changes ◽  
High Mobility ◽  
Gastric Cancer Cells ◽  
Dependent Cell ◽  
Pre Treatment ◽  
Endothelial Growth Factor

Accumulating evidence shows that curcumin exerts antitumor activities in a variety of malignancies. High mobility group box 1 (HMGB1) is associated with vascular endothelial growth factor D (VEGF-D)–induced lymphangiogenesis and tumor metastasis in gastric cancer. However, the molecular mechanisms by which curcumin regulates HMGB1-mediated lymphangiogenesis in gastric cancer remain unclear. In this study, the cytotoxic effects of curcumin were investigated in gastric cancer AGS and SGC-7901 cell lines by MTT assay, and curcumin-induced morphological changes and cell apoptosis were assessed by using flow cytometry analysis and caspase-3 activity. The effects of curcumin on HMGB1 and VEGF-D expression were examined by reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis. As a result, we found that curcumin decreased cell viability and caused a dose-dependent cell apoptosis through the activation of caspase-3. The mRNA and protein expression levels of HMGB1 and VEGF-D were significantly eliminated by curcumin administration. Pre-treatment with the recombinant HMGB1 (rHMGB1) markedly abolished curcumin-reduced VEGF-D expression. Our findings suggested that curcumin might exert anti-lymphangiogenesis in gastric cancer by inhibition of HMGB1/VEGF-D signaling.

Light activation of cyclometalated ruthenium complexes drives towards caspase 3 dependent apoptosis in gastric cancer cells

2020 ◽  
Vol 208 ◽  
pp. 111080 ◽  
Author(s):  
Jorge Andrés Solís-Ruiz ◽  
Anaïs Barthe ◽  
Gilles Riegel ◽  
Rafael Omar Saavedra-Díaz ◽  
Christian Gaiddon ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Ruthenium Complexes ◽  
Light Activation ◽  
Gastric Cancer Cells

scholarly journals Erk is involved in the differentiation induced by diallyl disulfide in the human gastric cancer cell line MGC803

2006 ◽  
Vol 11 (3) ◽  
Author(s):  
Hui Ling ◽  
Liang-Yun Zhang ◽  
Qi Su ◽  
Ying Song ◽  
Zhao-Yang Luo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Specific Activity ◽  
Lucifer Yellow ◽  
Gastric Cancer Cell Line ◽  
Major Constituent ◽  
Diallyl Disulfide ◽  
Human Gastric Cancer ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
Induced Differentiation

AbstractDiallyl disulfide (DADS) is a major constituent of garlic. Previously, we found that DADS both inhibited proliferation in human gastric cancer cells in vitro and in vivo, and induced G2/M arrest. In this study, we investigated whether this differentiation effect was induced by DADS in human gastric cancer MGC803 cells, and whether it was related to an alteration in ERK activity. The results showed that the growth of MGC803 cells was inhibited by DADS. Cells treated with DADS displayed a lower nucleocytoplasmic ratio and tended to form gland and intercellular conjunction structures. The ConA-mediated cell agglutination ratio and cells’ ALP specific activity decreased. In MGC803 cells, dye transfer was limited to a few cells neighbouring the dye-injected cell and to a depth of 1–2 layers beneath the scrape site. However, after treatment with DADS, the LY (Lucifer Yellow) was transferred to several cells immediately neighbouring the microinjected cell and to a depth of 2–4 cell layers from the scrape site. This indicated that DADS induced differentiation in MGC803 cells. Western blot analysis revealed that although DADS did not influence the quantity of ERK1/2 protein expressed, it did decrease its phosphorylation in a concentration-dependent manner, compared with the controls. At 30 mg·L−1, DADS inhibited the activation of ERK1/2 in 15–30 min. These results suggested that the DADS-induced differentiation of MGC803 cells involved an alteration of the ERK1/2 signaling pathway.

scholarly journals Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3

2001 ◽  
Vol 93 (6) ◽  
pp. 916-916 ◽  
Author(s):  
XH Jiang ◽  
BCY Wong ◽  
ST Yuen ◽  
SH Jiang ◽  
CH Cho ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Caspase 3 ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals PKM2 Is the Target of a Multi-Herb-Combined Decoction During the Inhibition of Gastric Cancer Progression

2021 ◽  
Vol 11 ◽  
Author(s):  
Qingmin Sun ◽  
Mengyun Yuan ◽  
Hongxing Wang ◽  
Xingxing Zhang ◽  
Ruijuan Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Nuclear Translocation ◽  
Aerobic Glycolysis ◽  
Metabolic Reprogramming ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition

Gastric cancer is the third leading cause of cancer death worldwide. Traditional Chinese medicine (TCM) is increasingly extensively applied as a complementary therapy for gastric cancer (GC) in China, which shows unique advantages in preventing gastric cancer metastasis. Previous study indicates modified Jian-pi-yang-zheng (mJPYZ) decoction inhibit the progression of gastric cancer by regulating tumor-associated macrophages (TAM). However, it is unclear whether mJPYZ can affect metabolic reprogramming of gastric cancer cells. Here, we showed that mJPYZ effectively attenuated GC cells proliferation, migration and invasion. Meantime, mJPYZ reduced the aerobic glycolysis level of GC cells in vivo and in vitro by regulating the expression and nuclear translocation of PKM2. Overexpression of PKM2 that could reverse the inhibitory effect of mJPYZ, migration and epithelial to mesenchymal transition (EMT). Our results showed PKM2/HIF-1α signaling was the key metabolic regulator of mJPYZ in GC cells. In summary, our present study suggested that abnormal PKM2 is required for maintaining the malignant phenotype of GC cells. The TCM decoction mJPYZ inhibited GC cells growth and EMT by reducing of glycolysis in PKM2 dependent manner. This evidence expanded our understanding of the anti-tumor mechanism of mJPYZ and further indicated mJPYZ a potential anti-tumor agent for GC patients.Chemical Compounds Studied in this ArticleRutin (PubChem CID: 5280805); Lobetyolin (PubChem CID: 53486204); Calycosin-7-glucoside (PubChem CID: 71571502); Formononetin (PubChem CID: 5280378); Calycosin (PubChem CID: 5280448); Ononin (PubChem CID: 442813); P-Coumaric Acid (PubChem CID: 637542).

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